糖皮质激素影响肉仔鸡骨骼肌脂肪代谢的机制研究.doc

糖皮质激素影响肉仔鸡骨骼肌脂肪代谢的机制研究 treatments: 1μM DEX, 100nM insulin, 1μM DEX+100nM insulin or control for 2 hours. Although not statistic significantly, DEX induced the increased mRNA level of AMPKα2 and L-CPT1, while decreased mTOR expression. The mRNA level of AMPKα 和 L-CPT1 were down-regulated by insulin. When cells were treated by cooperation of DEX and insulin, mRNA level of AMPKα2 and L-CPT1 were retarded, while mTOR expression was up-regulated. The result showed that fatty acid oxidation in myoblasts was improved by DEX, while decreased by insulin. The cooperation of DEX and insulin induced the retarded lipid utilization in chicken skeletam muscle. The pathway of glucocorticoids and insulin regulating lipid metabolism in chicken myoblast Myoblasts was prepared from SPF chicken embryos (11-d old), then subjected to following treatments: 1μM DEX, 10μM AMPK inhibitor, 100nM insulin, 20μM AKT inhibitor or control for 12 hours. The expressions of GR, AMPKa 2 and L-CPT1 were elevated while mTOR was decreased by DEX, and restored to normal by AMPK inhibitor, except for GR. AKT1 expression was not affected by DEX, but its expression was enhanced by AMPK inhibitor. Insulin induced the increased AKT1 and mTOR transcription and tended to decrease AMPKa 2 mRNA level, and they all restored to normal by AKT inhibitor. The results showed that DEX mediated myoblast lipid metabolism through regulation of AMPK and mTOR, independent of AKT, while insulin exert its effect via AKT-mTOR and AKT-AMPK-mTOR pathway. In conclusion, glucocorticoids administration distributes lipid to accumulation, rather than utilization. Glucocorticoids may promote intramyocellular lipid accumulation by increased fatty acid de novo synthesis and availability to tissue, in turn the decreased cellular AMP:ATP ratio. The following down-regulated AMPK induces the active mTOR signal, finally the retarded lipid oxidation. The elevated circulating insulin improves AKT1 pathway, but not associated with mTOR activation.